Most of the Reflex Sympathetic Dystrophy (RSD) or Complex Regional Pain Syndrome (CRPS Type 1) cases are diagnosed by clinical examination and lab studies. There are few cases, which may not show classical symptoms and sign during examination. Lab studies may be negative in some of these cases. Research study published in 1999 involving 134 patients suffering with RSD/CRPS Type 1 suggests, 53% of these patients had clinical and lab evidence of CRPS Type 1. These patients were interpreted as being consistent with the diagnosis of Reflex Sympathetic Dystrophy (RSD) or Complex Regional Pain Syndrome (CRPS Type 1).

Is It Possible To Develop A Symptom Of Reflex Sympathetic Dystrophy (RSD) or Complex Regional Pain Syndrome (CRPS Type 1) Following Minor Trauma?

Yes, minor injuries following trauma if not appropriately treated and associated with stressful events can cause RSD or CRPS Type 1. Study by Geertzen JH published in 1998 suggest 79.2% of the patient suffering with RSD or CRPS Type 1 had stressful life events.3 Trauma following auto or work accident is often associated with stressful events causing fear and anxiety.

Surgical skin incision in few cases may result in infection followed by inflammation. Untreated inflammation may develop in to RSD or CRPS Type 1. Postsurgical RSD is often seen in patients suffering with diabetes and end stage renal disease.4

RSD is not common among arthritis patient. Untreated inflammatory arthritis may be associated with symptoms of CRPS. Raynaud's disease and Charcot-Marie-Tooth disease are inflammatory arthritis, which in few cases are associated symptoms of RSD or CRPS Type 1 with vasomotor disorder secondary to dysfunction of autonomic nervous system.5, 6

What Is "Paraneoplastic Syndrome" In Cancer Patients?

RSD is frequently seen in patients suffering with cancer of skin and breast. Cancer is a debilitating disease. Spread of cancer damages surrounding normal soft tissue and bones resulting in inflammation. Such inflammation originating from cancer results in "Paraneoplastic Syndrome" because of hypersensitivity of surrounding nerve receptors and nerves resulting in RSD.7

Stroke is often associated with loss of consciousness in the initial stage and later loss of sensory and motor function of one or more than one limb. The extremity is at rest position for several days. Inactive limb shows signs of ischemic skin and muscle atrophy. Stroke also causes ischemia (lack of blood supply) to brain and pain centers resulting in hypersensitivity and abnormal secretion of pain transmitting chemicals result in symptoms of RSD.

Is Nerve Entrapment One Of The Causes Of Reflex Sympathetic Dystrophy (RSD) or Complex Regional Pain Syndrome (CRPS Type 1)?

Yes, median nerve entrapment caused by carpal tunnel syndrome is the best example of nerve entrapment resulting in RSD or CRPS Type 1. Similarly trigeminal nerve entrapment after brain surgery or dental procedures can result in trigeminal neuralgia a RSD like neuropathic pain.8

Center for Temporomandibular Disorders and Orofacial Pain, Department of Diagnostic Sciences, New Jersey

Dental School, UMDNJ, Newark, NJ 07103, USA.

Complex regional pain syndrome-like symptoms during herpes zoster.

Berry JD, Rowbotham MC, Petersen KL.

Pain. 2004 Jul;110(1-2):e1-12.

UCSF Pain Clinical Research Center, University of California, San Francisco 94115, USA.

Abstract:

However, only 13 cases have been published in the literature, and nothing is known about the incidence, prevalence, or natural history (Chester, 1992; Foster et al., 1989; Grosslight et al., 1986; Ketz and Schliack,1968; Kishimoto et al., 1995; Querol and Cisneros, 2001; Sudeck, 1901; Visitsunthorn and Prete, 1981). The aim of the present study was to determine the prevalence of CRPS-like symptoms in a prospectively gathered cohort of subjects with HZ and to follow the natural history of their pain and sensory disturbance during the first 6 months after onset of HZ. Subjects were evaluated at four time points after HZ: 2-6 weeks, 6-8 weeks, 3 months, and 6 months. Only subjects aged 50 or older with pain VAS ratings of >/=20/100 at 2-6 weeks were eligible. The first (screening) visit included a neurological and physical examination that was updated at each subsequent visit. Assessments included ratings of pain intensity, allodynia severity, and rash severity. The neurological exam included determination of presence or absence of the following CRPS-like symptoms: (1) increased sweating, (2) color changes, (3) skin temperature changes, (4) weakness of the affected area based on physical exam, (5) edema, and (6) extension of CRPS-like symptoms outside the affected dermatome. For subjects with HZ in dermatomes that can include the limbs (C4-T2 and L1-S2), extremity involvement was considered present if allodynia or rash extended beyond the neck of the humerus (upper extremity), the inguinal ligament (anterior lower extremity), or gluteal sulcus (posterior lower extremity). Involvement of the extremity was considered proximal if neither HZ rash nor allodynia extended past the elbow (upper extremity) or knee (lower extremity). Of the first 75 subjects recruited, 25 had HZ outbreaks in dermatomes that extended into the extremities (C4-T2 and L1-S2). In this group, 8 subjects had no extremity involvement, 8 had proximal extremity involvement, and 9 had distal extremity involvement. Subjects with distal extremity HZ reported more pain across the four visits (p < 0.05). At 3 months, more subjects with distal extremity involvement met criteria for PHN (8 out of 9, 89%), while only 4 out of 8 (50%) with proximal involvement and 2 out of 8 (25%) of subjects without extremity involvement met criteria for PHN (Chi-square test: p < 0.05). Only 25 out of the remaining 50 (50%) subjects with outbreaks in dermatomes that do not include the extremities met criteria for PHN at 3 months (Chi-square test: p < 0.05). Six months after onset of HZ, 6 out of 9 subjects with distal extremity involvement met PHN criteria compared with 2 out of 8 (25%) with proximal involvement and 2 out of 8 (25%) without extremity involvement (Chi-square test: p = 0.12). Fifteen out of 50 (30%) subjects with outbreaks in dermatomes that do not include the extremities met criteria for PHN (Chi-square test: p < 0.05). No subject had all six CRPS-like symptoms. Of the 17 subjects with extremity involvement, 9 subjects had '0-2 CRPS-like symptoms' and 8 had '3-5 CRPS-like symptoms'. None of the eight subjects without extremity involvement had any CRPS-like symptoms. Of the 50 subjects with HZ outside the extremity, only one had abdominal weakness. Pain ratings were higher in subjects with '3-5 CRPS-like symptoms'. More subjects with '3-5 CRPS-like symptoms' met criteria for PHN at 3 months (7 out of 8, 88%), compared to 5 out of 9 (55%) of subjects with '0-2 CRPS-like symptoms' (p = 0.07). At 6 months, 2 out of 9 (22%) of subjects with '0-2 CRPS-like symptoms' met criteria for PHN, compared with 6 out of 8 (75%) of subjects with '3-5 CRPS-like symptoms' (Chi-square test: p < 0.03). Two case-reports are presented. In summary, the occurrence of CRPS-like symptoms is common in subjects with HZ outbreaks affecting the extremity, particularly if the distal extremity is involved. It is uncertain if the pathophysiology underlying the CRPS-like symptoms observed in this study is similar to that of CRPS from other causes, or if it is relatively specific to HZ. Development of PHN is common in subjects who have experienced CRPS-like symptoms. More aggressive preventive treatments may be justified in this high-risk subset of HZ subjects to prevent development of PHN. Prospective randomized controlled studies are needed to determine which subjects are most likely to benefit and when treatment should begin.